Kinases are known to be important cellular enzymes that regulate cellular functions such as regulating cell division and proliferation. WO 2008/047307. Fms-like tyrosine 3 (FLT3) is a receptor tyrosine kinase (RTK) that is reported to be mutated in 25-30% of acute myeloid leukemia (AML) cases. See Miguel Sanz et al., “FLT3 inhibition as a targeted therapy for acute myeloid leukemia,” Current Opinion Oncol. (2009) 21:594-600. Specifically, a mutation in the internal tandem duplication (ITD) of the fms-like tyrosine 3 (FLT3) gene is reported to be the second most common genetic change associated with cytogenetically normal AML. This mutation is indicated to be an important prognostic factor for this class of patients as mutations of the ITD are associated with poor disease prognosis. Sanz Id. FLT3 is thus a recognized molecular target for the development of new therapies for AML. Sanz id at 596; Qi Chao et al, “Identification of . . . (AC220), a Uniquely Potent, Selective and Efficiacious FMS-Like Tyrosine Kinase-3 (FLT3) Inhibitor,” J. Med. Chem. (2009) 52:7808-7816. Currently, there are a number of selective FLT3 inhibitors being investigated as treatments for AML (including tandutinib and AC220), and sunitinib, a multitargeted kinase inhibitor (including FLT3), has already been approved for sale. See Chao et al., id; Sanz et al., supra. Other inhibitors of FLT3 that are in development are discussed in Sanz, id, and Thomas Fischer et al., J Clinical Oncol. (2010) 28:4339-4345.